Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011206 (delirium)
 5,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Delirium in children associated with high fever is defined as an acute and transient confusional state. Clinically it is most important to differentiate delirium from encephalitis or encephalopathy. Electroencephalographic (EEG) tracings were obtained from 17 children with fever and delirium, consisting of 12 boys and 5 girls, aged from 2 to 13 years. The initial recording was done from 2 to 36 hours (mean: 15 hours) after the last episode of delirium. The causes of fever were upper respiratory infections in 14 patients, acute bronchitis in 1, measles in 1 and exanthema subitum in 1. The body temperature ranged from 38.0 to 41.0 degrees C, when delirium was noticed by their parents. On 15 EEG tracings obtained during waking, the alpha rhythm showed a frequency normal for age, but it was interrupted by posterior slow waves in 2 of them. Eight tracings showed abnormal occipital delta activities. These slow waves were blocked by eye opening, and disappeared within 1 to 5 days. Two of the 6 tracings during sleep showed high voltage irregular slow wave bursts mixed with spikes lasting for 7 minutes, which also disappeared within 1 to 2 days. Our results indicate that EEG is useful in differentiating delirium from encephalitis or encephalopathy; in delirium, the occipital delta waves are blocked by eye opening and abnormal activities disappear within a few days.
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PMID:[Usefulness of EEG recording for delirium in children with high fever]. 1260 88

Infarction of the posterior cerebral artery may present only with signs of agitated delirium and an acute confusional state. In the absence of other prominent neurological deficits, this can be easily mistaken for toxic-metabolic encephalopathy, head trauma, post-ictal confusion, or a psychiatric disorder. Appropriate head imaging studies are important to detect an illness that might otherwise be missed and left untreated.
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PMID:Agitated delirium with posterior cerebral artery infarction. 1267 94

Children who present delirium associated with high fever may develop with encephalitis or encephalopathy, especially in influenza infection. The aim of this study is to differentiate the patients with the central nervous infection or with the parasomnias from benign transient delirium in patients who visit the emergency room complaining of illusions. Ten patients aged from 2 to 7 years were enrolled in this study. There were 2 patients with central nervous infection, one with encephalo-myelitis due to mycoplasma infection and one with acute necrotizing encephalopathy due to influenza infection. The remaining 8 patients had benign delirium associated with high fever which disappeared in a self-limiting manner. Three patients had a febrile seizure (FS) and 4 patients had family history of FS. The points to differentiate the delirium with parasomnias from benign type is fearful expression, positive past history, autonomic nerve symptoms. Delirium consisted of visual hallucination, and occurred in association with sleep except in the patients with encephalopathy who became delirious when they were awake. Abnormal neurological findings such as meningeal signs and disturbed consciousness, appearance of delirium in the waking state, and marked slowing in the EEG background activity were considered to be warning factors useful in differentiating the benign type from the delirium with central nervous infection.
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PMID:[Differential diagnosis in children having delirium associated with high fever]. 1287 7

We report a 53-year-old male patient with late onset mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes(MELAS) with hallucination and delusion. The patient manifested various neurological symptoms including perceptive deafness, muscle weakness of limbs with loss of consciousness, sensory abnormalities in hands, feet and a face, abnormal sense of taste, tremor, palsy of upward eye movement and weak deep tendon reflexes prior to the psychotic episode. He was diagnosed as MELAS, because of high serum lactic acid and pyruvic acid, and the point mutation in the mitochondrial DNA 3243. SPECT imaging showed decreased perfusion in occipital cortex and thalamus. These SPECT changes improved after disappearing visual hallucination. Hallucination might be caused by delirium due to stroke-like episode. Dysfunction in the occipital cortex and thalamus might be involved with this perfusion change.
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PMID:[A case with late-onset MELAS with hallucination and delusion]. 1523 27

The clinical characteristics and electroencephalogram (EEG) findings in delirious behavior in children with influenza were studied in order to differentiate it from influenza-associated encephalitis/encephalopathy. Fifteen consecutive children with delirious behavior associated with influenza were investigated. Their clinical courses were investigated using medical records. EEG was obtained during the delirious behavior, when possible. The body temperature during the delirious behavior was 39.0 degrees C or higher in 13 children. A subtle reduction of consciousness was observed in 10 children. Seizures were observed in five children. EEG revealed some mildly abnormal findings in 13 children, including mild slowing of the background activity, insertion of semirhythmic high voltage slow waves, and appearance of relatively high voltage semirhythmic theta waves. The EEG findings normalized after the delirious behavior had disappeared. EEG revealed transient and mild abnormalities in children with delirious behavior but without encephalitis/encephalopathy, and thus might be useful for diagnostic evaluation in such condition.
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PMID:Delirious behavior in children with influenza: its clinical features and EEG findings. 1586 89

Systemic lupus erythematosus (SLE) is an autoimmune disease that may involve the central nervous system (CNS) resulting in neuropsychiatric manifestations. The associated psychiatric disorders include depression, psychosis, mood disorders, anxiety, cognitive dysfunction, and delirium/ encephalopathy. Several autoantibodies may play a role in the pathogenesis of psychiatric complications of SLE, particularly antibodies against ribosomal P-proteins (anti-P) and possibly antibodies against endothelial cells (AECA). The reported prevalence of anti-P is highly variable in SLE patients and is dependent on different ethnic backgrounds, sensitivity and specificity of the assays employed for autoantibody detection, and the time at which sera were analysed in relation to the clinical event. Controversial data exist on the association of anti-P with psychiatric manifestations of SLE. These autoantibodies have been suggested to be specific markers of the psychiatric manifestations of SLE, particularly of the psychosis and depression, and the antibody level varied with the clinical activity of the disease. Some studies have confirmed the hypothesis of an association of anti-P antibodies with psychiatric manifestations of neuropsychiatric SLE (NPSLE) while others have disputed this relationship. This review summarizes the recent studies about relationship between anti-P antibodies and psychiatric manifestation of SLE.
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PMID:Anti-ribosomal P-protein and its role in psychiatric manifestations of systemic lupus erythematosus: myth or reality? 1617 27

Delirium and human immunodeficiency virus (HIV)-associated dementia are well recognized neuropsychiatric consequences of HIV infection in adults. Almost nothing is known regarding the management of delirium in HIV-infected children and adolescents. HIV-related progressive encephalopathy is thought to represent the pediatric form of HIV-associated dementia; however, this condition occurs in HIV-infected infants and preschool children and is rapidly followed by death. This report describes the identification and treatment of apparent HIV-associated dementia complicated by delirium in an adolescent girl.
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PMID:Case study: delirium in an adolescent girl with human immunodeficiency virus-associated dementia. 1683 11

Due to involvement of multiple systems, thallium poisoning is notorious for complexity and seriousness as symptoms of toxicity are non-specific and diverse. Alopecia and painful neuropathy are its cardinal features, others being gastrointestinal disturbances, encephalopathy, tachycardia, ataxia, hepatorenal and cardiac damage etc. We report a case of thallium poisoning who presented initially with gastrointestinal symptoms and later developed neurological features (peripheral neuropathy and delirium). Various diagnoses were entertained in this case and thallium poisoning was suspected only after he developed alopecia and neuropsychosis. He made a significant recovery by conservative management in spite of delay in diagnosis. We conclude that a high level of suspicion should be kept for thallium poisoning, especially in patients with painful, peripheral neuropathy and gastrointestinal symptoms which appear earlier than alopecia, since prognosis is more rewarding with early diagnosis, leading to complete recovery.
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PMID:Thallium poisoning presenting as paresthesias, paresis, psychosis and pain in abdomen. 1664 41

In daily hospital activity a frequent observation is that of patients in conditions of acute global suffering of the central nervous system due to a primary cause or symptomatic of other diseases. This condition shows an alteration of the state of consciousness, which involves three possible semeiologic manifestations: delirium (acute confusional state), acute confusional state associated with psychomotor underactivity and coma. The possible causes of an acute encephalopathy (AE) are: metabolic, iatrogenic and toxic, infective, primary neurologic, surgery-related and others. Diagnostic-therapeutic routes to be followed by emergency room doctors and neurologists dealing with AE are defined.
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PMID:Acute encephalopathies. 1670 87

Beyond the cerebral impact of cardiac arrest, recent research indicates a high prevalence of neurological disturbances such as delirium and coma among patients admitted to the intensive care unit (ICU). These disturbances, grouped here under the term "encephalopathy," may be overlooked while attention is devoted to reversing life-threatening imbalances in cardiac and pulmonary function. Nevertheless, there is ample evidence that encephalopathy is an independent predictor of mortality. Factors associated with encephalopathy include primary cerebral disorders such as stroke, trauma, and meningitis, or systemic derangements including sepsis, organ failure, and exposure to pharmacological agents and toxins. Although encephalopathy may resolve with treatment of the underlying disorder, there is mounting evidence that cerebral dysfunction persists beyond the acute phase of critical illness. ICU survivors often suffer chronic impairments in cognitive ability, suggesting occult brain injury. The pathogenesis and natural history of encephalopathy, still poorly understood, need further clarification to spur the development of effective preventive and therapeutic interventions.
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PMID:The spectrum of encephalopathy in critical illness. 1696 45


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